Abstract
Background Bu-zhong-yi-qi granule (BZYQ), a sort of Chinese herbal medicine, has exhibited therapeutic effects on ulcerative colitis (UC). However, the mechanism of BZYQ has not been fully clarified. This study was aimed at investigating the effects of BZYQ on UC rats model and at exploring its potential mechanism. Methods The UC rats were established by enema of trinitrobenzene sulfonic acid (TNBS). The therapeutic effects of BZYQ treatment were evaluated by disease activity index (DAI), colon macroscopic damage index (CMDI) scores, and histological observation. The mRNA levels of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-10 (IL-10) were measured by quantitative real time-polymerase chain reaction (qPCR). The expression of tight junction (TJ) proteins, occludin and claudin-1, in the colon was determined by Western blot and immunofluorescence. The expression of toll-like receptors 4 (TLR4), nuclear factor-kappa B (NF-κB), p-NF-κB, myosin light chain kinase (MLCK), MLC, and p-MLC levels in colon was determined by Western blot or qPCR. Results The results showed that BZYQ could attenuate DAI, CMDI, and histological inflammation. TJ proteins expression was decreased in UC rats, but treatment with BZYQ restored the expression of occludin and claudin-1. In addition, BZYQ administration ameliorated UC-associated increase in the production of TNF-α, IL-1β, and the expression of TLR4, NF-κB, p-NF-κB, MLCK, MLC, and p-MLC, while BZYQ administration increased the production of IL-10. Conclusions The therapeutic effect of BZYQ on UC is at least partially through regulation of the secretion of some inflammatory cytokines and improvement of TJ integrity via TLR4/NF-κB/MLCK pathway.
Highlights
Ulcerative colitis is a chronic idiopathic inflammatory bowel disease characterized by persistent mucosal inflammation beginning in the rectum and extending to the proximal end
To further evaluate the effects of Bu-zhong-yi-qi granule (BZYQ) treatment, we investigated the role of toll-like receptors 4 (TLR4), NF-κB, p-NF-κB, myosin light chain kinase (MLCK), myosin light chain (MLC), and p-MLC in ulcerative colitis (UC) inflammation and tight junction integrity
Our present study proved that BZYQ was effective in treating UC in rats, and the underlying therapeutic mechanisms of BZYQ, maybe the regulation of the TLR4 pathway, suppressed MLCK expression and the activity of NF-κB, while there was a subsequent increase in the expression levels of occludin and claudin-1
Summary
Ulcerative colitis is a chronic idiopathic inflammatory bowel disease characterized by persistent mucosal inflammation beginning in the rectum and extending to the proximal end. Recent experimental evidence implicates a crucial function of barrier dysfunction in the onset of inflammatory bowel disease [6]. E therapeutic effects of BZYQ treatment were evaluated by disease activity index (DAI), colon macroscopic damage index (CMDI) scores, and histological observation. E expression of tight junction (TJ) proteins, occludin and claudin-1, in the colon was determined by Western blot and immunofluorescence. E expression of toll-like receptors 4 (TLR4), nuclear factor-kappa B (NF-κB), p-NF-κB, myosin light chain kinase (MLCK), MLC, and p-MLC levels in colon was determined by Western blot or qPCR. E therapeutic effect of BZYQ on UC is at least partially through regulation of the secretion of some inflammatory cytokines and improvement of TJ integrity via TLR4/NF-κB/MLCK pathway Conclusions. e therapeutic effect of BZYQ on UC is at least partially through regulation of the secretion of some inflammatory cytokines and improvement of TJ integrity via TLR4/NF-κB/MLCK pathway
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